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Perinatal Exposure to Bisphenol a Exacerbates Nonalcoholic Steatohepatitis-Like Phenotype in Male Rat Offspring Fed on a High-Fat Diet

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Perinatal Exposure to Bisphenol a Exacerbates Nonalcoholic Steatohepatitis-Like Phenotype in Male Rat Offspring Fed on a High-Fat Diet JWEI, X SUN and others Maternal BPA exposure and 222:3 313–325 Research hepatic steatosis Perinatal exposure to bisphenol A exacerbates nonalcoholic steatohepatitis-like phenotype in male rat offspring fed on a high-fat diet Jie Wei2,*, Xia Sun1,*, Yajie Chen1, Yuanyuan Li, Liqiong Song, Zhao Zhou, Bing Xu, Yi Lin1 and Shunqing Xu Key Laboratory of Environment and Health, Ministry of Education and Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Correspondence Huazhong University of Science and Technology, Wuhan 430030, China should be addressed 1Key Laboratory of Urban Environment and Health, Department of Environmental and Molecular Toxicology, to S Xu or Y Lin Institute of Urban Environment, Chinese Academy of Sciences, Xiamen 361021, China Emails 2Department of Basic Medical Sciences, Medical College, Xiamen University, Xiamen 361102, China [email protected] or *(J Wei and X Sun contributed equally to this work) [email protected] Abstract Bisphenol A (BPA) is one of the environmental endocrine disrupting chemicals, which is Key Words present ubiquitously in daily life. Accumulating evidence indicates that exposure to BPA " bisphenol A Journal of Endocrinology contributes to metabolic syndrome. In this study, we examined whether perinatal exposure " steatosis to BPA predisposed offspring to fatty liver disease: the hepatic manifestation of metabolic " insulin resistance syndrome. Wistar rats were exposed to 50 mg/kg per day BPA or corn oil throughout " oxidative stress gestation and lactation by oral gavage. Offspring were fed a standard chow diet (SD) or a " inflammation high-fat diet (HFD) after weaning. Effects of BPA were assessed by examination of hepatic " fibrosis morphology, biochemical analysis, and the hepatic expression of genes and/or proteins involved in lipogenesis, fatty acid oxidation, gluconeogenesis, insulin signaling, inflam- mation, and fibrosis. On a SD, the offspring of rats exposed to BPA exhibited moderate hepatic steatosis and altered expression of insulin signaling elements in the liver, but with normal liver function. On a HFD, the offspring of rats exposed to BPA showed a nonalcoholic steatohepatitis-like phenotype, characterized by extensive accumulation of lipids, large lipid droplets, profound ballooning degeneration, impaired liver function, increased inflam- mation, and even mild fibrosis in the liver. Perinatal exposure to BPA worsened the hepatic damage caused by the HFD in the rat offspring. The additive effects of BPA correlated with higher levels of hepatic oxidative stress. Collectively, exposure to BPA may be a new risk factor for the development of fatty liver disease and further studies should assess whether this finding is also relevant to the human population. Journal of Endocrinology (2014) 222, 313–325 http://joe.endocrinology-journals.org Ñ 2014 Society for Endocrinology Published by Bioscientifica Ltd. DOI: 10.1530/JOE-14-0356 Printed in Great Britain Downloaded from Bioscientifica.com at 09/25/2021 11:58:55PM via free access Research JWEI, X SUN and others Maternal BPA exposure and 222:3 314 hepatic steatosis Introduction Nonalcoholic fatty liver disease (NAFLD) is one of the free fatty acid (FFA) composition as well as upregulation of typical hepatic manifestations of metabolic syndrome genes involved in lipid biosynthesis (Marmugi et al. 2012). characterized by hepatic fat accumulation in the absence Most importantly, this study revealed a nonmonotonic of excess alcohol consumption. NAFLD affects 15–40% of dose–response curve in which lower doses of BPA (doses the general population in Western countries and 9–40% of within one order of magnitude of approximately 50 mg/kg people in Asian countries (Farrell & Larter 2006). A subset per day) were more effective than the higher dose of patients with NAFLD may progress to nonalcoholic (5000 mg/kg per day) for altering lipid biosynthesis steatohepatitis (NASH), a more severe form of hepatic pathways. damage associated with inflammation, fibrosis, cirrhosis, Exposure to an adverse environment during critical or hepatocellular carcinoma (Farrell & Larter 2006). In windows of development will affect the programing of addition to genetic and diet-related factors, exposure to metabolically active tissues in offspring, predisposing environmental pollutants has been shown to negatively individuals to metabolic disorders later in life. For example, affect key pathogenic events implicated in NAFLD. For maternal nutrient excess or restriction has been confirmed instance, chronic inhalation of low levels of ambient air to increase the risk of NAFLD in the offspring (McCurdy particulate matter (PM 2.5) has been was reported to et al. 2009, Bayol et al. 2010, Oben et al. 2010). For BPA, induce hepatic steatosis and lipid peroxidation and, results from several studies using animal models indicated moreover, increase hepatic inflammatory and fibrosis that metabolic disorders were observed in offspring when stage in mice (Tomaru et al. 2007, Tan et al. 2009). they were exposed to BPA during the critical period of Exposure to nitrosamines and nicotine has also been development. Perinatal exposure to BPA altered early found to play critical roles in the pathogenesis of NAFLD adipogenesis and increased the body weight of offspring (Tong et al. 2009, Azzalini et al. 2010, Friedman et al. 2012). (Rubin & Soto 2009, Somm et al. 2009). A brief exposure to Bisphenol A (BPA) is a well-known environmental BPA during pregnancy has also been found to initiate endocrine disrupting chemical, which is used extensively insulin resistance in adult offspring (Alonso-Magdalena in the manufacture of products containing epoxy resins et al. 2010). Consistent with these findings, results from our and polycarbonate, such as toys, food and beverage previous study have confirmed that perinatal exposure to containers, paper currency, etc. (Diamanti-Kandarakis BPA resulted in a higher body weight and body fat Journal of Endocrinology et al. 2009). Humans can be exposed to BPA present in percentage, a greater mass of white adipocytes, hyperlipi- commonly used products. Recently, growing evidence has demia, hyperleptinemia, and insulin intolerance in adult indicated that exposure to BPA is associated with an rat offspring (Wei et al. 2011). All of these detrimental increased risk of some metabolic diseases such as obesity, effects of BPA might increase the risk of NAFLD. insulin resistance, type 2 diabetes, dyslipidemia, etc. In this study, we employed a developmental BPA (Alonso-Magdalena et al. 2011, Shankar et al. 2012, Vom exposure paradigm in rats to test the hypothesis that Saal et al. 2012). The presence of these metabolic disorder perinatal exposure to BPA caused a predisposition to events has been documented to predict the future hepatic steatosis. Our findings supported this hypothesis development of NAFLD (Fan et al. 2005, Hamaguchi and further indicated that perinatal exposure to BPA et al. 2005). Indeed, a recent epidemiological study has coupled with the postweaning high-fat diet (HFD) related BPA exposure to abnormal concentrations of the significantly initiated hepatic oxidative stress, thereby liver enzymes g-glutamyltransferase (gGT) and alkaline predisposing offspring to hepatic inflammation and early phosphatase (ALP), two of the sensitive markers for fibrosis in adulthood. hepatocellular damage (Lang et al. 2008). In addition, K K low concentrations of BPA (10 4–10 12 M) have been reported to induce lipid accumulation and steatosis in Materials and methods hepatic HepG2 cells by disturbing mitochondrial function Ethics and releasing proinflammatory cytokines (Huc et al. 2012). An animal study also confirmed that oral exposure of adult Allanimalexperimentswere carried out humanely male CD1 mice to BPA (0, 5, 50, 500, and 5000 mg/kg per following the guidelines for the care and use of animals day) resulted in the accumulation of hepatic triglycerides established by Tongji Medical College and were approved (TGs) and cholesteryl esters (CHOL), changes in hepatic by the Ethics Committee of Tongji Medical College. http://joe.endocrinology-journals.org Ñ 2014 Society for Endocrinology Published by Bioscientifica Ltd. DOI: 10.1530/JOE-14-0356 Printed in Great Britain Downloaded from Bioscientifica.com at 09/25/2021 11:58:55PM via free access Research JWEI, X SUN and others Maternal BPA exposure and 222:3 315 hepatic steatosis Animals (CAT) and glutathione S-transferase (GST)) in hepatic tissue homogenates were detected using the correspond- Wistar rats were housed in polypropylene cages with ing assay kits (Nanjing Jiancheng Bioengineering Insti- free access to food and water under standard conditions tute, Nanjing, China). (22G2 8C, 12 h light:12 h darkness cycles). Glass water bottles were used to avoid potential contamination from sources other than administration. Pregnant female rats Liver function tests m were administered corn oil or 50 g/kg per day BPA by oral At the age of 27 weeks, blood was collected from the orbital gavage from gestational day 0 to postnatal day 21. Offspring sinus in rat offspring for serum measurements following were culled to five males and five females in each litter after 16 h of fasting. The liver biomarkers, namely alanine delivery and were nursed with their own mother. After aminotransferase (ALT), aspartate aminotransferase (AST), weaning, offspring were supplied with a standard chow diet ALP, and gGT, were assayed using commercially available
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